Diffuse Traumatic Subarachnoid Hemorrhage Mimicking Aneurysmal Bleeding Secondary to Ophthalmic Artery Avulsion: Case Report and Review of the Literature.

BACKGROUND: Traumatic subarachnoid hemorrhage (SAH) is a common finding following traumatic brain injury. In some cases, it can be associated with hydrocephalus. This type of hemorrhage is mostly caused by the rupture of small vessels in the brain and is usually managed conservatively. CASE DESCRIPTION: We present a case of a 60-year-old woman who presented with traumatic luxation of the eye following a fall. This resulted in diffuse SAH (Fisher grade IV) with associated hydrocephalus. We also report on 3 previous similar cases found in the literature. Avulsion of the ophthalmic artery was found to be the cause of the traumatic SAH. Apart from cerebrospinal fluid diversion using an external ventricular drain, the case was managed conservatively. There was no evidence of delayed clinical or radiologic vasospasm. CONCLUSIONS: Traumatic avulsion of the ophthalmic artery may result in diffuse SAH, mimicking that of aneurysmal rupture. This case shows that management of early complications, such as hydrocephalus and seizures, should be the main aim. Surgical or endovascular treatment of the injured artery, however, would be unnecessary.

Analysis of biochemical laboratory values to determine etiology and prognosis in patients with subarachnoid hemorrhage: a clinical study.

OBJECTIVES: The aim of this study was to establish prognostic and predictive markers in patients with subarachnoid hemorrhage (SAH) using simple laboratory methods. METHODS: A retrospective examination was made of patients with SAH diagnosed secondary to isolated head trauma, isolated anterior communicating artery aneurysm rupture, and angiography-negative SAH. Age, gender, Glasgow Coma Scale (GCS) scores, and Fisher's grade scores, Glasgow Outcome Scale (GOS) scores, leukocyte count, neutrophil count, lymphocyte count, platelet count, neutrophil-lymphocyte ratio (NLR) and platelet-lymphocyte ratio results (PLR) were evaluated. RESULTS: NLR and PLR values, which were similar in patients with spontaneous SAH, were significantly high in patients with traumatic SAH. NLR and PLR values could be 80% sensitive and 75% specific for distinguishing traumatic SAH from spontaneous SAH. Eosinophil count was lower in patients with angiography-negative SAH and patients with aneurysmal SAH than in patients with traumatic SAH. Initially measured GCS score, Fisher's grade score, eosinophil, neutrophil and lymphocyte counts could be prognostic in all patients with SAH. Moreover, it was concluded that the initially measured number of eosinophils might be directly related to patient prognosis. The eosinophil count was generally found to be high in traumatic SAH patients and it was observed that this parameter could be predictive for these patients. Lymphocyte count and NLR values could be prognostic markers in patients with angiography-negative SAH. CONCLUSION: NLR, PLR and eosinophil count values could be predictive for etiological factors (traumatic SAH or spontaneous SAH) of patients who were admitted unconscious to the emergency room with SAH detected on radiological imaging.

Triage Patterns of Traumatic Subarachnoid Hemorrhage: Is Referral to a Tertiary Care Center Necessary?

OBJECTIVE: Isolated traumatic subarachnoid hemorrhage (iTSAH) in mild head injuries has more evidence that triage to a tertiary care facility, intensive care unit admission, and repeat imaging is not warranted. Certain factors were identified that predict radiographic and clinical progression in hopes of preventing avoidable cost, which occur with transfer and subsequent management. METHODS: A retrospective analysis identified 67 patients transferred between January 2010 and December 2014 who met inclusion criteria. Primary outcomes assessing neurosurgical intervention, radiographic, and clinical progression were documented. Secondary outcomes included any operative intervention, length of stay, standardized hospital costs, disposition at discharge, and 30-day mortality. RESULTS: The mean age of the cohort was 67.7 ± 16.4 years, with most patients (82.1%) having a Glasgow coma score of 15. Warfarin was used in 10 patients (14.9%), although 55.2% were on an antiplatelet or anticoagulation agent. No patient required neurosurgical intervention. One patient, on clopidogrel (Plavix) and warfarin, neurologically declined with radiographic progression. Older age seem to correlate with radiographic progression (P = 0.05). Dementia (P = 0.05) as well as warfarin use (P = 0.06) correlated with clinical progression. Cost in patients without other injuries was associated with warfarin use (P = 0.0002), injury severity scores (P = 0.01), and initial Glasgow coma score (P = 0.0003) on multivariate analysis. CONCLUSIONS: In this series of patients with mild traumatic brain injury, the rate of neurological deterioration due to expansion of iTSAH in patients is low, regardless of the use of antiplatelets/anticoagulants. Triage to a tertiary care facility generally is not warranted and can prove costly to patients with iTSAH without other injures.

Delayed Deterioration in Isolated Traumatic Subarachnoid Hemorrhage.

BACKGROUND: Isolated traumatic subarachnoid hemorrhage (SAH) in association with mild traumatic brain injury is considered to be a less severe finding that is not likely to require surgical intervention. No previous reports have described cases warranting craniotomy for isolated traumatic SAH by itself. CASE DESCRIPTION: We report 2 cases of minor head trauma with isolated traumatic SAH that showed delayed clinical deterioration requiring immediate surgical intervention. Initial computed tomography showed isolated traumatic SAH in the basal cistern and Sylvian fissure in both cases. Angiography showed no aneurysmal source. Within 24 hours of each accident, both disturbance of consciousness and hemiparesis deteriorated. Follow-up computed tomography showed formation of intracerebral hematoma adjacent to the Sylvian fissure. Intraoperative findings showed abruption injury of a perforating branch arising from the middle cerebral artery (MCA) as the cause of bleeding. Impact at the time of injury could have caused traction on the MCA in the Sylvian fissure, resulting in abruption of the perforator. CONCLUSIONS: Isolated traumatic SAH seen in the basal cistern and Sylvian fissure carries a risk of late deterioration. A possible cause of hematoma expansion is abruption of a perforating branch arising from the MCA at the time of head injury. When hematoma expansion is identified, surgical evacuation of the hematoma is indicated. Surgical evacuation should be safely performed with the knowledge of the point of bleeding in such patients.

Subarachnoid hemorrhage in ten questions.

Traumatic subarachnoid hemorrhage (SAH) has an annual incidence of 9 per 100 000 people. It is a rare but serious event, with an estimated mortality rate of 40% within the first 48hours. In 85% of cases, it is due to rupture of an intracranial aneurysm. In the early phase, during the first 24hours, cerebral CT, combined with intracranial CT angiography is recommended to make a positive diagnosis of SAH, to identify the cause and to investigate for an intracranial aneurysm. Cerebral MRI may be proposed if the patient's clinical condition allows it. FLAIR imaging is more sensitive than CT to demonstrate a subarachnoid hemorrhage and offers greater degrees of sensitivity for the diagnosis of restricted subarachnoid hemorrhage in cortical sulcus. A lumbar puncture should be performed if these investigations are normal while clinical suspicion is high.

Delayed post-traumatic large subgaleal hematoma caused by diastasis of rhomboid skull suture on the transverse sinus.

PURPOSE: This study aimed to consider an appropriate treatment for large subgaleal hematoma with skull fracture and epidural hematoma (EDH). CASE REPORT: A 6-year-old boy presented at our hospital with head trauma, and computed tomography (CT) showed a thin EDH in the right temporo-occipital area and cranial diastasis in the right lambdoidal suture. However, no neurological deficits were identified in the patient. One week after trauma, he visited our hospital again with a massive fluctuant watery mass extending from the forehead to the right temporoparietal areas, and laboratory data revealed that he was anemic. CT showed a massive subgaleal hematoma with extremely high density around the cranial diastasis. Damage of the transverse sinus was suspected, and emergent sinus repair surgery was performed. The surgery disclosed that bleeding from the transverse sinus was flowing out extracranially through the cranial diastasis. The subgaleal and epidural hematomas were removed, and bleeding from the sinus was stopped by dural tacking sutures along the transverse sinus. Postoperative CT demonstrated complete disappearance of epidural and subgaleal hematomas. The patient recovered from general fatigue without blood transfusion and was discharged 9 days after surgery. CONCLUSIONS: The therapeutic strategy for massive subgaleal hematoma is individualized. However, treatment for massive subgaleal hematoma with skull fracture should not be considered the same as for hematoma without skull fracture. Emergent surgery is recommended before neurological deterioration is recognized in the patient if damage to the dural sinus is suspected.

The nonsurgical nature of patients with subarachnoid or intraparenchymal hemorrhage associated with mild traumatic brain injury.

OBJECT: Mild traumatic brain injury (mTBI), as defined by Glasgow Coma Scale (GCS) score of 13 or higher, is a common problem in the United States and worldwide, estimated to affect more than 1 million patients yearly. When associated with intracranial hemorrhage, it is a common reason for neurosurgical consultation and transfer to tertiary care centers. The authors set out to investigate the clinical implications of subarachnoid hemorrhage (SAH) and/or intraparenchymal hemorrhage (IPH) associated with mTBI in hopes of standardization of mTBI clinical care and optimization of resource allocation. METHODS: The authors performed a retrospective review of 500 consecutively treated patients with mTBI and SAH and/or IPH admitted to a Level I trauma center in Alabama between May 2003 and May 2013. They performed a review of medical records to confirm the diagnosis, determine neurological condition at admission, and assess for episodes of neurological decline or brain injury-related complications including altered mental status, seizures, and hyponatremia. RESULTS: Of the 500 patients for whom data were reviewed, 304 (60.8%) were male and 196 (39.2%) were female. Average age was 46.3 years. Overall, 63 patients (12.6%) had isolated IPH, 411 (82.2%) had isolated SAH, and 26 (5.2%) had radiographic evidence of both IPH and SAH. One hundred forty-five patients (29%) were transferred an average distance of 64.5 miles. The authors identified no patients who experienced neurological worsening during their hospital course. Two patients experienced hyponatremia that required treatment with sodium supplementation. CONCLUSIONS: Patients with the constellation of SAH and/or IPH and mTBI do not require neurosurgical consultation, and these findings should not be used as the sole criteria to justify transfer to tertiary referral centers.

Does isolated traumatic subarachnoid hemorrhage merit a lower intensity level of observation than other traumatic brain injury?

Evidence is emerging that isolated traumatic subarachnoid hemorrhage (ITSAH) may be a milder form of traumatic brain injury (TBI). If true, ITSAH may not benefit from intensive care unit (ICU) admission, which would, in turn, decrease resource utilization. We conducted a retrospective review of all TBI admissions to our institution between February 2010 and November 2012 to compare the presentation and clinical course of subjects with ITSAH to all other TBI. We then performed descriptive statistics on the subset of ITSAH subjects presenting with a Glasgow Coma Score (GCS) of 13-15. Of 698 subjects, 102 had ITSAH and 596 had any other intracranial hemorrhage pattern. Compared to all other TBI, ITSAH had significantly lower injury severity scores (p<0.0001), lower head abbreviated injury scores (p<0.0001), higher emergency department GCS (p<0.0001), shorter ICU stays (p=0.007), higher discharge GCS (p=0.005), lower mortality (p=0.003), and significantly fewer head computed tomography scans (p<0.0001). Of those ITSAH subjects presenting with a GCS of 13-15 (n=77), none underwent placement of an intracranial monitor or craniotomy. One subject (1.3%) demonstrated a change in exam (worsened headache and dizziness) concomitant with a progression of his intracranial injury. His symptoms resolved with readmission to the ICU and continued observation. Our results suggest that ITSAH are less-severe brain injuries than other TBI. ITSAH patients with GCS scores of 13-15 demonstrate low rates of clinical progression, and when progression occurs, it resolves without further intervention. This subset of TBI patients does not appear to benefit from ICU admission.

Intravenous paracetamol for fever control in acute brain injury patients: cerebral and hemodynamic effects.

BACKGROUND: Fever occurs frequently in acute brain injury patients, and its occurrence is associated with poorer outcomes. Paracetamol, an antipyretic frequently employed in patients with cerebral damage, may cause hypotension. We evaluated the cerebral and hemodynamic effects of intravenous (IV) paracetamol for the control of fever in Neuro-Intensive Care Unit (NICU) patients. METHODS: This is a prospective observational study in which we enrolled 32 NICU patients: Subarachnoid Hemorrhage (SAH, n = 18), Traumatic Brain Injury (TBI, n = 10), Intracerebral Hemorrhage (ICH, n = 2) and Acute Ischemic Stroke (AIS, n = 2). RESULTS: The administration of paracetamol resulted in a decrease of core body temperature (Tc) (p = 0,0001), mean arterial pressure (MAP) (p = 0,0006), cerebral perfusion pressure (CPP) (p = 0,0033), and jugular venous oxygen saturation (SjVO2) (p = 0.0193), and in an increase of arteriojugular venous differences of oxygen (AVDO2) (p = 0.0012). The proportion of patients who had an infusion of norepinephrine increased from 47 % to 75 % (p = 0.0039 McNemar Test). When intracranial pressure (ICP) at the start of paracetamol infusion (t-0) was compared with the measurement of ICP after 2 h, a significant correlation was observed (r = 0.669, p = 0.0002). This marked and significant correlation can be explained by the fact that for the higher levels of ICP assessed at t-0 (greater than 15 mmHg), we observed a marked reduction of ICP concomitant with the decrease of Tc. No problems related to norepinephrine administration and/or increase in dosage were observed. CONCLUSION: Paracetamol administration is effective but exposes patients to hypotensive episodes that must be recognized and treated expeditiously to prevent further damage to the injured brain.

Patients with traumatic subarachnoid hemorrhage are at low risk for deterioration or neurosurgical intervention.

BACKGROUND: Current standard of care for patients with traumatic intracranial hemorrhage (TIH) includes neurosurgical consultation and/or transfer to a trauma center with neurosurgical backup. We hypothesize that a set of low-risk criteria can be applied to such patients to identify those who may not require neurosurgical evaluation. METHODS: This is a cross-sectional study of consecutive emergency department patients in 2009 and 2010 with TIH on computerized tomographic scan owing to blunt head trauma. Patients presented to an urban academic Level I trauma center (volume, 92,000) were older than 15 years and had a Glasgow Coma Scale (GCS) score of 13 or greater. Charts were abstracted using a standardized data form by two emergency physicians. Our principal outcome was deterioration represented by a composite of neurosurgical intervention, clinical deterioration, or worsening computerized tomographic scan result. RESULTS: During the study period, 404 patients were seen with TIH and met our inclusion criteria, and 48 of those patients (11.8%) deteriorated. Patients with isolated subarachnoid hemorrhage, were less likely to deteriorate (odds ratio [OR], 0.08; 95% confidence interval [CI], 0.011-0.58). Characteristics associated with deterioration were subdural hematomas (OR, 2.63; 95% CI, 1.198-5.81) or presenting GCS of less than 15 (OR, 2.12; 95% CI, 1.01-4.43).The use of anticoagulant medications or antiplatelet agents were not associated with deterioration for warfarin, aspirin, or clopidogrel; however bleeding diatheses were corrected with vitamin K, fresh frozen plasma, and platelets as necessary. CONCLUSION: Patients with isolated traumatic subarachnoid hemorrhage are at low risk for deterioration. These individuals may not need neurosurgical consultation or transfer to a trauma center where neurosurgical backup is available. Those patients with subdural hematoma or a GCS of less than 15 have a higher risk of deterioration and require neurosurgical evaluation. LEVEL OF EVIDENCE: Therapeutic/care management, level IV.

The impact of traumatic subarachnoid hemorrhage on outcome: a study with grouping of traumatic subarachnoid hemorrhage and transcranial Doppler sonography.

BACKGROUND: To clarify the clinical role of traumatic subarachnoid hemorrhage (tSAH), stratified analysis with grouping of tSAH was performed. Their blood flow changes and correlations with outcome were assayed. METHODS: One hundred seventeen tSAH patients were classified into several groups according to their initial computerized tomography scans. Group I included patients with tSAH only in the posterior interhemispheric fissure, whereas Group II contained patients with tSAH located elsewhere. Group II was further subdivided into IIa, little SAH; IIb, extensive SAH; IIc, little SAH with intraventricular hemorrhage (IVH); and IId, extensive SAH with IVH. The cerebral blood flow velocity was monitored using transcranial Doppler sonography (TCD). RESULTS: Both age and initial coma scale were independent predictors of poor outcome. The poor outcome rates in various subgroups of tSAH increased stepwise from group I to group IId (I, 7.4%; IIa, 18.4%; IIb, 33.3%; IIc, 62.5%; and IId, 90.9%) (p = 0.0010). Stratified analyses revealed that patients with extensive tSAH (group IIb + IId) were more likely to have unfavorable outcomes (47.7%) than patients with little tSAH (group IIa + IIc) (26.1%) (p = 0.0185); patients with IVH (group IIc + IId) also displayed a higher incidence (78.9%) of poor outcomes than patients without IVH (group IIa + IIb) (25.4%) (p = 0.0030). TCD study demonstrated that patients with extensive tSAH (group IIb + IId) were more likely to have the vasospasm based on TCD criteria than did patients in group I and group IIa + IIc (37.5% vs. 5.9% and 7.7%, p = 0.0105). Notably, there was a tendency of worse outcome in patients with vasospasm on the basis of TCD-derived criteria than those without, with the unfavorable outcome rates being 47.4% and 24.7% (p = 0.0799). CONCLUSIONS: Age, initial coma scale, extensive tSAH, and IVH are independent predictors of poor outcome in the cohort of tSAH patients. Statistically, patients with extensive tSAH are significantly more likely to have vasospasm.

[Injuries to the upper cervical medulla in severe brain injuries]. / Verletzungen des oberen zervikalen Myelons beim schweren Schädel-Hirn-Trauma.

BACKGROUND: Cranial magnetic resonance imaging (MRI) was performed in 250 patients who had been unconscious post-trauma for at least 24 hours. The frequency and the characteristics of injuries to the upper cervical myelon were determined. PATIENTS AND METHODS: Between 1996 and 2009, MRI was carried out within 8 days of trauma. RESULTS: No lesions of the upper cervical medulla were found without accompanying damage to the medulla oblongata. Two groups were found to have a lesion in the upper cervical myelon. (i) In 3.2 % of the patients in a state of deep coma MRI revealed lesions in the entire brain stem. These died without waking from coma. (ii) 2 % of the patients were found to have additional damage to the distal medulla oblongata. These victims of high-speed traumas awoke from coma after 2-3 days. They revealed frontal contusions of the brain and traumatic subarachnoidal hemorrhages. Injuries to the bony upper cervical spine and/or the skull base were frequent. Four of them died, one patient survived with severe disabilities. CONCLUSION: Two types of lesions involving the upper cervical myelon could be differentiated, both of which occur only in association with lesions in the medulla oblongata.